We know pleural effusion (hydrothorax) is disproportionately more common on right side in cardiac failure.Though its a well observed phenomenon, the mechanism of which has not been clear to us. It could be due to multiple anatomical , physiological factors.

*The are right and left lymphatic (Thoracic) ducts that drain the corresponding lungs and pleural space . There can be overlap and contribute to the differential occurrence of pleural effusion

Reference

A meticulous paper written some 75 years ago (1946) from Harvard medical school teach us some important points in this phenomenon.

There is still lot, to be understood about pleural effusion in cardiac failure. We need to know why some pleural effusions tend to occur independent of hydrostatic forces. It is also noted long-standing transudative effusions can become true exudates. Role of local pleural capillary hypoxia resulting increasing permeability is underestimated.Hepatic congestion and trans-abdominal seepage of fluid is a distinct possibility.

One more area we are not clear is the relationship between the genesis of pericardial effusion in cardiac failure and concomitant pleural effusion. Post operatively , after univentricular repair (as in Fontan ), pleural effusions can be much problematic with high venous pressure interfering with pleural drainage.

Impact on symptoms

Finally, even mild pleural effusion can increase the work of breathing and result in dyspnea which is out of proportion to cardiac dysfunction.While we expect the diurteics to clear the effusion of cardiac failure, it doesn’t happen always arguing for a non transudative mechanism in at least some of them.

Further reading

Discerned readers are advised to study the pleural space dynamics in detail.

Reading X -ray chest can be as blind as a bat flying in the dark . It needs lots of Imagination . (Many times the blindness continues to cath lab as well during structural interventions is a different story !)

Yes ,its true any one can recognise a cardiomegaly in X-ray . . . but Which chamber is responsible for cardiomegaly ? and quantifying each ones contribution to the increased CTR is the critical question.

We know the 4 chambers in the heart are arranged in a complex pre-specified (Antero -superior and right to left orientation ) still , the CT ratio in X-RAY chest is based on the diameter formed by two chambers only ie right atrium and left ventricle.

However, any of the 4 chamber enlargement can increase CT ratio in pathological conditions.

LV enlargement is the most common cause for cardiomegaly as it is the normally border forming.(DCM, Aortic valve, HT diseases)

RV can do it when it enlarger grossly forming the left heart border(COPD, Severe pulmonary hypertension of any cause)

RA can enlarge to both pressure and volume overload.(CHF, with RVF)

LA is least likely to be border forming as it is midline structure .Since It tends to enlarge posteriorly and superiorly it rarely enlarges sideways. Occasionally In severe mitral stenosis it can enlarge to the right and cross the right heart border causing the classical shadow in shadow.

Since I have struggled with X ray orientation of heart chambers in my early days (Still i do sometimes!) Just thought , why we are not fusing a X-ray with a given patients echocardiogram that will help understand the chamber anatomy .

Note : The Left atrium is not only left of RA , its also posterior and superior to RA.This makes the IAS not actually pure right left to relationship but also a slight infero to superior and antero posterior orientation.(This can be realised when we puncture the IAS from RA side the needle goes more of superior)

X ray chest left lateral view is fused with para- sternal long axis view. Please note this is not true anatomical correlates. The RV shown in echo is actually RVOT but in X-ray its more of RV body .

* A note of caution : The fused Images are rough attempt to co-register x-ray with echo. There is sophisticated software in some new generation cath labs to mix fluro images with live TEE data that aid in Interventions.

Postample
A bedside Instant point of care echo is becoming a norm in clinical cardiology practice. Why bother about X-ray then ? Agreed to that point to a certain extent. But, I used to tell my (amused ) students that technology based lazy learning doesn’t help build a strong scientific foundation which would ultimately threaten the patient care one day !

Heart is not like a rigid structure built with bricks . . . . so , its too architectural mindset to describe cardiac chambers to be made up of walls. Rather , Its a four chambered muscle mass moulded together in a complex 3D interface with distinct surfaces rather than walls. It’s also important to realise, since the heart is positioned (rather hanging )delicately in the middle mediastinum resting on the diaphragm , its subjected to one more dynamism due to respiratory motion blurring the definition of surfaces as well. (Vertical vs Horizontal)

Posterior surface is now referred to as infero-posterior

The posterior aspect of heart contains essentially the venous channels and the atrium (LA in particular)pulmonary veins and coronary sinus. This happens right from 8 week heart open stage when venous end of lower straight heart tube folds up and posteriorly .

It should be recalled only a small portion of lower aspect of posterior wall is alloted to left ventrilce.Instead the Infero diaphragmatic surface is formed by two-thirds the LV and one-third Right ventricle.

Image courtesy : From the great Netter

Nomenclature issue

The term posterior wall is now abandoned in most Echocardiography texts its replaced by inferior .The implication is more for Electrophysiologists with reference to accessory pathway localization

What is true posterior wall MI ?

As discussed before ,posterior surface of heart is different from posterior aspect of left and and right ventricle.

What does leads V7 V8 V9 record ?

It actually records electrical signals arising from posterior aspect of heart. Left atrium, pulmonary vein along with insulatory effect of lungs dampens the potential . This makes the sensitivity of ST elevation in posterior MI is low.

Syncope and seizure are most dramatic symptoms that rarely fails to call the attention of the patient and family.Syncope is primarily evaluated at medical or cardiac units. However ,when syncope presents as convulsions (often It is ! ) the patient lands up in a Neuro unit as a case of epilepsy.Some how, many of them are prescribed anti convulsants without being evaluated for what triggered the seizure.

Real life experience now suggest, a bothering number of patients in epilepsy clinic might harbor a primary cardiac disorder in the form of either brady or tachycardia which is often inherited due to defect in ion channels of cardiac cell.

Incidence of sudden cardiac death in patients with seizure disorder though rare is being increasingly recognised. Mechanical problems like valvular Aortic stenosis can also result in syncope followed by seizure.

Final message

Cardiologists do have a major role these situations.It may be wise to advice basic cardiac work up in every seizure disorder. As we are beginning to understand the neurogenic triggers in sudden cardiac deaths , the need for Neuro-Cardiac units is real.(Some of big university hospitals do have such departments)

There are important diseases that restricts entry of blood into right heart chambers. They can occur either in an acute (Tamponade) or in chronic fashion like constrictive pericarditis and restrictive cardiomyopathy.These entities show distinctive impact on JVP and systemic pulse.

The two pathognomonic signs are Kussmaul sign and pulsus paradoxus* that go hand in hand in most situations.Inappropriate elevation of JVP with inspiration is termed as Kussmaul sign , while exaggerated fall in systemic BP with inspiration is called Pulsus paradoxus.The later is the arterial counter part of Kussmaul sign in JVP .However, there can be dissociation between these two signs occasionally.

* Pulsus paradoxus is a term originally used by Kussmaul when he noted heart sounds were retained while pulse dissappeared in patients with cardiac tamponade .Later we realised the loss of pulse was linked to inspiratory cycle of respiration. To make this sign objective sphygmomanometery criteria was formulated which measured the difference between inspiratory and expiratory korotkoff’s sounds .

Coming up next

Why Kussmaul sign is often absent in Tamponade while its arterial counterpart pulsus paradoxus may still be conspicuous ?

We know aortic regurgitation causes a deluge of hugely popular peripheral signs of aortic run off , which are taught right from 2nd year medical school.

When the aorta leaks it reflects in the entire vascular tree .How is that a leak in the remote aortic valve cause a quincke’s to and fro pulsations in the finger pulp ?

Is the blood in the finger trying to follow the regurgitant jet that go back into left ventricle ? Does the to and fro murmur of Duroziez over the femoral artery imply there is reversal of blood flow in femoral artery ?

Things are little complex than it appears

It is true the initiating event of collapsing pulse is the regurgitant jet , however the mechanism that amplifies and sustains it , lies in the altered peripheral hemodynamics.

The systemic arteriolar resistance is dramatically low in chronic severe AR by a reflex phenomenon , as cardiac out put is increased and vascular tree adopt to it. So, with each beat when blood is ejected two things happen in diastole .While a small fraction runs back into LV , the rest of blood runs off , as if it goes in a free way making all peripheral pulses dynamic , bounding and collapsible.

Hence as the name suggest all the peripheral signs of AR are due to the peripheral mechanisms rather than primary event of aortic run off into left ventricle.

Why carotid pulse does not show the collapsible nature of pulse in AR ?

If aortic leak into LV is the dominant mechanism , carotid artery should obviously manifest a collapse ,but it doesn’t ,as carotid has no direct continuity with the peripheral low resistance circuit

What is the hemo-dynamic correlates of descending aortic flow reversal in severe AR ?

The central vascular tree manifest some reversal till the regurgitant velocity fades off . This can occur in severe AR, extending into certain length of aorta. This can be picked up by Doppler probe. Please realise it is only the wave form that get reversed not the actual blood stream.( The momentum gained in systole continues to push forward in-spite of the pulling back forces of regurgitation)

Why peripheral signs are absent in acute AR ?

Acute AR even if it’s significant does not cause a collapsing pulse because it takes time for the peripheral vascular tree to go for vasodilatory mode.Further ,LV is also less compliant keeping the LVEDP high and regurgitant fraction low.

Summary

Answering the title question ,the mechanism of Aortic run off in AR is both central and peripheral. However clinical signs are largely due to high cardiac out put and the resultant adaptive response of the vascular tree due to low systemic vascular resistance triggered by reflex dilatation of small arteriolesof the peripheral vascular bed.

When a patient comes with angina at rest , it could mean two things .Either a STEMI or an NSTEMI .This , we can diagnose only after seeing the ECG .

Can we differentiate these two by the character of chest pain alone ?

Very tough task isn’t ? But there are some definite clues .

Infarct pain

Is mostly sudden .

Likely to be crescendo , lasts more than 20-30 minutes .

Fails to get relived by rest or even Nitrites.

Sweating due to sympathetic activation is more pronounced.

Unstable angina

Is rarely sudden .Often has a pro-drome.

UA is mostly precipitated by an increased demand situation or a stress.

It has a typical waxing and waning pattern . Rarely assume a true crescendo character as myocytes does not necrose (Just threaten to die !)

The chest pain radiation to shoulder is less conspicuous , instead it tends to reach the jaw area .(* An observation,Is it something to do with multi-vessel CAD in UA ?)

Mechanism of the difference : Epicardial vs Endocardial angina

The pain of UA is due to subtotal occlusion and endocardial ischemia , while STEMI is sudden total occlusion and the resultant transmural ischemia . In STEMI epicardial surface is always involved (Which lifts the ST segment in ECG .).We know epicardium is same as visceral layer of pericardium which is well innervated .Hence pain of STEMI acquires more of somatic character than a predominately visceral type pain that occurs with UA/NSTEMI where epicardial ischemia is absent.

Clinical importance

The demarcation between unstable angina and Infarct pain becomes vital when we calculate the time window for thrombolysing STEMI .Many of them have a phase of pre infarction angina which is a type of unstable angina. If we mistake it for Infarct pain then one may falsely calculate a prolonged time window and deny re-perfusion therapy.

Post -amble

It is tricky issue to differentiate the chest pain of STEMI and NSTEMI .A significant overlap can occur in real coronary care scenario . We know chest pain that occurs in both pre and post infarct phase is considered as unstable angina .(With infarct pain sandwiched between them!) Hence differentiating them may even be termed as futile.

Still,clinical cardiology can be made fascinating by indulging in such exercise !